RESUMO
Following the publication of the above article, the authors contacted the Editorial Office to explain that the strips of ßactin, LC3 and p62 proteins of the RKO cell line shown in Fig. 2A and B, and those of the SW620 cell line shown in Fig. 3A and B, were assembled in these figures incorrectly. To rectify the presentation of these two figures, the authors proposed that they replace the strips of ßactin and p62 proteins in the original Figs. 2B and 3B with the ßactin bands from one of the repeated western blotting experiments. The revised and corrected versions of Figs. 2 and 3 are shown on the next page. The authors wish to emphasize that these corrections do not grossly affect either the results or the conclusions reported in this work. The authors all agree to the publication of this Corrigendum, and are grateful to the Editor of Oncology Reports for granting them the opportunity to correct the errors that were made during the assembly of these figures. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [Oncology Reports 45: 86, 2021; DOI: 10.3892/or.2021.8037].
RESUMO
p53reactivation and induction of massive apoptosis1, APR017 methylated (PRIMA1met; APR246) targets mutant p53 to restore its wildtype structure and function. It was previously demonstrated that PRIMA1met effectively inhibited the growth of colorectal cancer (CRC) cells in a p53independent manner, and distinctly induced apoptosis by upregulating Noxa in p53mutant cell lines. The present study including experiments of western blotting, acridine orange staining and transmission electron microscopy revealed that PRIMA1met induced autophagy in CRC cells independently of p53 status. Importantly, PRIMA1met not only promoted autophagic vesicle (AV) formation and AVlysosome fusion, but also increased lysosomal degradation. Furthermore, Cell Counting Kit8 assay, colony formation assay and small interfering RNA transfection were performed to investigate the underling mechanisms. The study indicated that activation of the mTOR/AMPKULK1Vps34 autophagic signaling cascade was key for PRIMA1metinduced autophagy. Additionally, autophagy served a crucial role in the inhibitory effect of PRIMA1met in cells harboring wildtype p53, which was closely associated with the increased expression of Noxa. Taken together, the results determined the effect of PRIMA1met on autophagy, and further revealed mechanistic insights into different CRC cell lines. It was concluded that PRIMA1metbased therapy may be an effective strategy for CRC treatment.